Tooth hypersensitivity is a common problem which affects about 40 million adults in the United States, 10 million of which can be considered chronically affected (Kanapka, Dent. Clin. North Am., 34:54, 1990). It is estimated that some 17% of adults in the U.S. have at least one or more sensitive teeth. The teeth may be sensitive to cold, heat, air or sweet foods.
The incidence of tooth hypersensitivity increases with age. The increased incidence is believed to be related to the general increase in exposed root surfaces of the teeth resulting from periodontal disease, tooth brush abrasion or cyclic loading fatigue of the thin enamel near the dento-enamel junction.
One theory to explain tooth hypersensitivity is based on the belief that open dentinal tubules allow fluid flow through the tubules. The flow excites the nerve endings in the dental pulp. Clinical replicas of sensitive teeth viewed in the scanning electron microscope (SEM) reveal varying numbers of open or partially occluded dentinal tubules.
Tubules generally are not seen at the tooth root surface because the cementum covering the tooth root or a smear layer of dentinal debris 2-5 .mu.m in thickness that covers the tooth surface masks the tubules. When the smear layer of the tooth is present, the fluid flow that can occur through the dentin is only a few percent of that possible following acid removal of the smear layer, which treatment "opens" the tubules.
There is a growing body of evidence that occlusion of the dentinal tubules of a sensitive tooth, whether by resin infiltration, varnish coat or more recently by crystallite precipitation, results in reduction or elimination of hypersensitivity. The duration of relief, however, is highly variable. Hypersensitivity usually reappears because of tooth brush abrasion, the presence of acid challenges in the mouth or degradation of the coating material.
A two-step procedure for reducing hypersensitivity, involving application of a calcium nitrate solution and a potassium phosphate solution to the tooth, was believed to produce calcium phosphate crystals which were believed to occlude tubules (Kaminske et al., J. Dent. Res., 69:68, 1990).
Increasing concentrations of oxalic acid in the food bolus by including foods high in oxalic acid in the diet, up to 1.14 g/l of oxalic acid resulting in a pH of about 2, yielded precipitation of a deposit at the tooth surface. A maximal response was found at a level of 0.1% (w/v) oxalic acid equivalents. However, greater levels of oxalic acid did not yield greater protection of the teeth. It was postulated that the deposited material was calcium oxalate resulting from interaction of the oxalic acid with calcium in the saliva (Gortner et al., J. Nutr., 32:121, 1946), although the level of calcium in saliva is very low.
Alkali metal or ammonium oxalate also has been used to reduce tooth hypersensitivity. The low pH of about 2 of the solution is believed to mobilize calcium and phosphate from the hard tissues (U.S. Pat. No. 4,057,621).
In addition, a 3.0% (w/v) monohydrogen monopotassium oxalate solution, usually having a pH of about 2, was found to occlude dentinal tubules (Pashley et al., Arch. Oral. Biol., 23:1127, 1978). However, on closer examination, that treatment regimen deposited very few crystals on the dentin surface or within the tubules, and the deposited crystals are removed readily by water irrigation (Knight et al., J. Periodontol., 64:366-373, 1993). Minimal crystal precipitation and poor adherence of the crystals to dentin were confirmed independently.
Desensitizing dentifrices containing potassium oxalate have been found to provide temporary tubule occlusion (Pashley et al., J. Periodontol., 55:522, 1984). Potassium oxalate is thought to react with the smear layer to increase the resistance thereof to acid attack, as well as to reduce fluid permeability. It was thought that calcium oxalate crystals were produced when the dentin was treated with potassium oxalate (Pashley et al., Arch. Oral Biol., 30:731, 1985).
A two-component kit comprising a first 1-30% (w/v) neutral oxalate solution, such as dipotassium oxalate, and a second subsequent 0.5-3% (w/v) acidic oxalate solution, such as monopotassium-monohydrogen oxalate with a pH of 2 or as low as 1, has been described. It is alleged that the neutral oxalate forms large crystals over the dentinal surface and the acidic oxalate forms smaller crystals around and about the previously formed larger crystals, so as to form a combined layer of microscopic crystals (U.S. Pat. No. 4,538,990). However, examination of dentin surfaces subjected to treatment by the two-component kit described in U.S. Pat. No. 4,538,990 were found essentially to be free of deposited crystals and the tubules were non-occluded or open.
Studies on the occlusion of dentinal tubules by deposition of crystals from potassium oxalate-based media (30% (w/v) K.sub.2 C.sub.2 O.sub.4 and 3% (w/v) KHC.sub.2 O.sub.4) showed variable results, purportedly due to variations in the size and number of crystals generated by the two solutions. The rate of crystal formation was alleged to be influenced by the local Ca.sup.2+ ion concentration, and it was stated that the acidic 3% (w/v) solution of KHC.sub.2 O.sub.4 with a pH of about 2 generates an extremely high local calcium ion concentration by etching the tooth, allegedly resulting in accelerated formation of abundant crystals (Muzzin et al., J. Periodont., 60:151, 1989).
An effective two-step method of sealing dentinal tubules is the subject of copending application Ser. No. 08/282,960 filed Aug. 1, 1994. However, for reasons of clinical expediency, there is need for an effective and efficient one-step procedure for sealing dentin tubules.
A one-step method for occluding dentinal tubules, PROTECT.TM. (J. O. Butler, Chicago, Ill.), involves the application of a 3% (w/v) aqueous solution of KHC.sub.2 O.sub.4 having a pH of about 2 to the tooth surface. The solution does not contain calcium salts because it is believed that etching of the tooth structure by the reagent contributes a more than adequate supply of Ca.sup.2+ to enable sufficient precipitation and crystal formation, when the compound is applied to the tooth surface or in the tubule. However, it was observed that PROTECT.TM. has limited effectiveness because many tubules remain open.
A 6% (w/v) ferric oxalate in nitric acid solution having a pH of about 3 and a dentin bonding product known as TENURE.TM., which is a 3% (w/v) aluminum oxalate in nitric acid solution with a pH of about 1, were found to be insufficient in achieving adequate dentinal tubule occlusion and pain relief.